ArticleMolecular and cellular biochemistry2022
Tannic acid attenuate AKT phosphorylation to inhibit UMUC3 bladder cancer cell proliferation.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Exploring the Mechanism of Tannic Acid AgainstPathogens (Basel, Switzerland) · 2026Article
- Post-translational modifications: Principal regulators of bladder cancer.Molecular biology reports · 2026Review
- Research progress on the role of AGC kinase family in bladder cancer.Discover oncology · 2025Review
- Antitumor and Antiangiogenic Effect of Tannic Acid in the Advanced Stage of Ehrlich Ascites Tumor in Mice.International journal of molecular sciences · 2025Article
- Nanomedicine's shining armor: understanding and leveraging the metal-phenolic networks.Journal of nanobiotechnology · 2025Review
- Integrated network pharmacology, molecular docking and experimental validation to investigate the mechanism of tannic acid in nasopharyngeal cancer.Scientific reports · 2025Article
- The Emerging Role of Natural Products in Cancer Treatment.Archives of toxicology · 2024Review
- Study of the FeACS omega · 2023Article
- Impact of SOX2 function and regulation on therapy resistance in bladder cancer.Frontiers in oncology · 2022Review
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
Abstract
Urothelial bladder cancer is rapidly spreading across Western countries, and therapy has shown little-to-moderate effects on bladder cancer. Thus, focusing on curbing cancer incidence has become crucial. The aim of the present study was to investigate the anticancer effects of Tannic acid (TA) in human bladder cancer. UMUC3 bladder cancer cells were treated with different concentrations of TA (0-100 µM) and tested for cell viability, colony formation, and apoptosis. The involvement of the phosphoinositide-3 kinase (PI3K)/Akt pathway in the action of TA was examined. TA treatment significantly inhibited the viability and increased percentage of apoptotic cells, thereby decreasing antiapoptotic proteins (BCL2, MCL-1, and BCL-XL) expression, resulting in the Caspase-3 activation. TA treatment decreased stem cell markers expression such as SOX2, OCT4, and NANOG. Additionally, TA treatment significantly reduced the phosphorylation levels of Akt in bladder cancer cells. Our study demonstrates the growth inhibitory effects of TA in bladder cancer cells, and highlights its potential as an anticancer agent for bladder cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.